ArticleProceedings. Mathematical, physical, and engineering sciences2023
Computational modelling distinguishes diverse contributors to aneurysmal progression in the Marfan aorta.
Article in Proceedings. Mathematical, physical, and engineering sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Computational multiscale analysis of growth and remodeling in the ascending aorta of the Marfan mouse.Biomechanics and modeling in mechanobiology · 2026Article
- The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Cardiovascular research · 2026Review
- Hypertension drives thoracic aortic aneurysm and dissection in male, but not female, Marfan mice.Journal of the mechanical behavior of biomedical materials · 2026Article
- Growth arrest of thoracic aortic aneurysms in aging Marfan mice.American journal of physiology. Heart and circulatory physiology · 2026Article
- Mechanics and mechanobiology of arterial development.Biomechanics and modeling in mechanobiology · 2026Review
- A multiscale computational model of ascending thoracic aortic aneurysm development in Marfan syndrome for in silico trials.Biomechanics and modeling in mechanobiology · 2026Article
- Mechanisms driving thoracic aortic aneurysm instability.Biomechanics and modeling in mechanobiology · 2026Article
- Mechanisms Driving Thoracic Aortic Aneurysm Stability.bioRxiv : the preprint server for biology · 2025Article
- Importance of localized dilatation and distensibility in identifying determinants of thoracic aortic aneurysm with neural operators.PLoS computational biology · 2025Article
- Computational modelling distinguishes diverse contributors to aneurysmal progression in the Marfan aorta.Proceedings. Mathematical, physical, and engineering sciences · 2023Article
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4 authors.
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Abstract
Thoracic aortic aneurysms are characterized by a progressive loss of biomechanical functionality resulting from degenerative changes in wall composition, microstructure, and mechanical properties. Among the many causes of these lesions, Marfan syndrome is the most common heritable condition, resulting from mutations to the gene that codes the elastin-associated glycoprotein fibrillin-1. Key histopathological features of the aneurysmal Marfan aorta include extensive degradation of elastic fibres, significant remodelling of fibrillar collagens and compromised smooth muscle cell function. Computational growth and remodelling models have confirmed the importance of compromised elastic fibre integrity in aneurysmal dilatation, but we show here that this contributor alone is not sufficient to describe biomechanical data collected from the two most common mouse models of Marfan syndrome. Rather, our simulations suggest that compromised mechanosensing and mechanoregulation of extracellular matrix by mural cells also play central roles in the natural history. Determination of optimal disease-contributing parameters further suggests a rapid reduction in cellular mechanosensing and mechanoregulation relative to diminished elastic fibre integrity, highlighting the importance of inter- and intra-lamellar elastin in the Marfan aorta. Aneurysmal dilatation in Marfan syndrome thus results from multiple contributors to progressive degeneration of the aortic wall, and computational mechanobiological models can help disentangle these contributions.
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